Altered Serum Bile Acid Pattern as an Independent Factor for Covert and Overt Hepatic Encephalopathy in Patients With Cirrhosis.

Authors

Takao Miwa, Hajime Ueda, Teruo Miyazaki, Akira Honda, Tadashi Ikegami, Shinji Unome, Tatsunori Hanai, Yohei Shirakami, Masahito Shimizu

Published in

Hepatology research : the official journal of the Japan Society of Hepatology. Sep 27, 2025. Epub Sep 27, 2025.

Abstract

Bile acid (BA) signaling plays an important role in the pathogenesis of hepatic encephalopathy (HE), including covert (CHE) and overt HE (OHE). However, few studies have examined its clinical impact in patients with cirrhosis.
This retrospective study included patients with cirrhosis who underwent CHE assessment using a computer-aided neuropsychiatric test. BAs were quantified using liquid chromatography-tandem mass spectrometry. Patients were divided into high and low groups according to their BA levels. Independent factors, namely CHE, OHE development, and mortality, were assessed using logistic, Fine-Gray competing risk, and Cox proportional hazards regression models.
Among the 189 patients, the median age was 71 years, 74.1% were male, and 28.0% were diagnosed with CHE. During a median follow-up period of 3.1 years, 15.9% (n = 30) developed OHE, and 33.3% (n = 63) died. Considering mortality as a competing risk, multivariable analysis identified a high conjugated primary BA level (subdistribution hazard ratio [HR] 3.44; 95% confidence interval [CI] 1.08-10.97) as an independent factor for OHE development. Additionally, a high non-conjugated primary BA level (odds ratio 2.18; 95% CI 1.06-4.46) was an independent factor of CHE. Furthermore, a high conjugated primary BA level (HR 2.06; 95% CI 1.11-3.83) was an independent predictor of mortality.
Elevated serum conjugated primary BA levels are an independent factor for OHE development and mortality in patients with cirrhosis. Additionally, elevated non-conjugated primary BA levels were an independent factor for CHE in these patients.

PMID:
41014583
Bibliographic data and abstract were imported from PubMed on 28 Sep 2025.

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